Evidence map›Paper›PMID 17438291›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

The same genomic region conditions clonal deletion and clonal deviation to the CD8alphaalpha and regulatory T cell lineages in NOD versus C57BL/6 mice.

Phillip D Holler, Tetsuya Yamagata, Wenyu Jiang, Markus Feuerer, Christophe Benoist, Diane Mathis

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. CD8ααSkin health and disease · 2021
    Article
  2. Distinct PLZFJournal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  3. Alloactivation of Naïve CD4Frontiers in immunology · 2019
    Article
  4. Article
  5. Foxp3 expression in T regulatory cells and other cell lineages.Cancer immunology, immunotherapy : CII · 2014
    Review
  6. Thymic negative selection is functional in NOD mice.The Journal of experimental medicine · 2012
    Article
  7. Article
  8. Article
  9. Article
  10. The defect in T-cell regulation in NOD mice is an effect on the T-cell effectors.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  11. Review
  12. Enhanced thymic selection of FoxP3+ regulatory T cells in the NOD mouse model of autoimmune diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Phillip D HollerSection on Immunology and Immunogenetics, Joslin Diabetes Center;
Tetsuya Yamagata
Wenyu Jiang
Markus Feuerer
Christophe Benoist
Diane Mathis
Harvard University · USBrigham and Women's Hospital · USJoslin Diabetes Center · US

Funding

AIRE, a zinc-finger protein that controls autoimmunityR01DK060027 · NIDDK · JOSLIN DIABETES CENTER · PI DIANE J MATHIS · 2002 to 2026
$7.4M
Aire, a zinc-finger protein that controls autoimmunityR37DK060027 · NIDDK · HARVARD MEDICAL SCHOOL · PI MATHIS, DIANE J · 2011 to 2015
$1.9M
NIDDK NIH HHS DK 60027NIDDK NIH HHS R01 DK060027NIDDK NIH HHS R37 DK060027
6 · The paper itself

Abstract

Clonal deviation is a mechanism by which immature thymocytes expressing a self-reactive T cell antigen receptor (TCR) are rescued from clonal deletion by adopting an alternative differentiation pathway resistant to apoptosis. Here, we confirm and generalize previous indications that genetic alleles in NOD mice condition ineffective clonal deviation toward the CD8alphaalpha lineage, a peculiar population of TCRalphabeta lymphocytes that electively colonizes the intraepithelial lymphocyte pool in the gut. Thymic selection of CD8alphaalpha cells was very age-dependent, occurring almost exclusively in the postnatal period. Fewer CD8alphaalpha cells were found in the thymus and intraepithelial lymphocytes of BDC2.5 TCR transgenic mice on the NOD than on the C57BL/6 (B6) background; this paucity extended to standard NOD mice, albeit to a lesser extent. CD8alphaalpha cells resided in the BDC2.5 pancreatic infiltrate, and they were more abundant on the B6 than the NOD background, correlating with aggressivity of the lesion. A (B6(g7) x NOD)F(2) intercross in agonist-challenged BDC2.5 fetal thymic organ cultures demonstrated the existence of a major quantitative trait locus on chromosome 3, coincident with an interval associated with resistance to clonal deletion. A replicate linkage confirmed these positions and showed that the same region also controls clonal deviation toward the CD4(+)FoxP3(+) regulatory T cell lineage. That clonal deviation toward the CD8alphaalpha and regulatory T cell pathways share genetic control further highlights the similarities between these two "rescue lineages," consistent with an immunoregulatory role for CD8alphaalpha cells.

Indexed as

Cell LineageAnimalsCD8 AntigensChromosome MappingClonal DeletionGenomeImmunity, InnateMiceMice, Inbred C57BLMice, Inbred NODPeptidesRNA, MessengerT-Lymphocytes, RegulatoryCD8 antigen, alpha chainCD8 AntigensPeptidesRNA, Messenger

Identifiers

PMID17438291
PMCPMC1855402
OpenAlexW1999760992

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.